We have recently shown that the level of plasma immunoglobulin is important in controlling the degree of binding of activated complement components to targets. The immunoglobulin is believed to act as a receptor for these activated components preventing their attachment to the antibody coated targets. It appears that one major effect of intravenous immunoglobulin used for therapeutic use is to raise the level of circulating immunoglobulin. This has no effect on complement activation but diverts attack away from targets. Patients have been administered IVIG and their serum has been shown to be less effective at lysing antibody coated target cells or red cells from patients with paroxysmal nocturnal hemoglobinuria, cells that are highly complement susceptible. Patients with either auto- immune hemolytic anemia or idiopathic thrombocytopenic purpura have been treated with IVIG, known to be therapeutic. The level of red cell IgG rose since the IVIG has anti red cell antibodies. The levels of red cell C3 fell and the patients improved. Myeloma proteins have been show to vary in their ability to prevent complement attack on targets. The structural basis for the difference between proteins is under study.